This shows you the differences between two versions of the page.
Both sides previous revisionPrevious revisionNext revision | Previous revisionNext revisionBoth sides next revision | ||
home:pathogenesis:vitamind:metabolism [03.29.2017] – [Bacteria disable the VDR] + ref. sallieq | home:pathogenesis:vitamind:metabolism [01.01.2019] – [Metabolism of vitamin D and the Vitamin D Receptor] sallieq | ||
---|---|---|---|
Line 3: | Line 3: | ||
A number of studies have suggested that patients with chronic inflammatory diseases are deficient in 25-hydroxyvitamin-D (25-D) and that consuming greater quantities of vitamin D, which elevates 25-D levels, alleviates symptoms of disease. Some years ago, molecular biology identified 25-D as a secosteroid. Secosteroids would typically be expected to depress inflammation, | A number of studies have suggested that patients with chronic inflammatory diseases are deficient in 25-hydroxyvitamin-D (25-D) and that consuming greater quantities of vitamin D, which elevates 25-D levels, alleviates symptoms of disease. Some years ago, molecular biology identified 25-D as a secosteroid. Secosteroids would typically be expected to depress inflammation, | ||
- | Located in the nucleus of a variety of cells including immune cells, the VDR is a control system of sorts. When exposed to infection and damage, especially that which is caused by pathogens, the body begins to convert the inactive form 25-D into the active form, 1,25-D. As cellular concentrations of 1,25-D increase, 1,25-D activates the VDR, turning on any number of genes the receptor transcribes. | + | Located in the nucleus of a variety of cells including immune cells, the VDR is a control system of sorts. When exposed to infection and damage, especially that which is caused by pathogens, the body begins to convert the inactive form 25-D into the active form, 1,25-D. As cellular concentrations of 1,25-D increase, 1,25-D activates the VDR, turning on any number of genes the receptor transcribes. |
According to a 2010 analysis, the VDR significantly affects 229 human genes. Many of these genes have long been associated with autoimmune diseases and cancers including, for example, the genes IRF8 (linked to multiple sclerosis), and PTPN2 (connected to Crohn' | According to a 2010 analysis, the VDR significantly affects 229 human genes. Many of these genes have long been associated with autoimmune diseases and cancers including, for example, the genes IRF8 (linked to multiple sclerosis), and PTPN2 (connected to Crohn' | ||
Line 92: | Line 92: | ||
==== Mechanisms by which bacteria affect levels of 25-D and 1,25-D ==== | ==== Mechanisms by which bacteria affect levels of 25-D and 1,25-D ==== | ||
- | < | + | < |
{{section>: | {{section>: | ||
Line 116: | Line 116: | ||
< | < | ||
- | * **synovial fluid surrounding the joints of patients with rheumatoid arthritis** – Mawer //et al// found that 1,25-D levels were particulary | + | * **synovial fluid surrounding the joints of patients with rheumatoid arthritis** – Mawer //et al// found that 1,25-D levels were particularly |
* **immune cells including macrophages** – Research has also shown that 1,25-D is synthesized in cells of the immune system, including the T cells and antigen-presenting cells(({{pubmed> | * **immune cells including macrophages** – Research has also shown that 1,25-D is synthesized in cells of the immune system, including the T cells and antigen-presenting cells(({{pubmed> | ||
Line 225: | Line 225: | ||
{{topic> | {{topic> | ||
+ | |||
+ | ===== Read more research ===== | ||
+ | |||
+ | {{https:// | ||
+ | |||
+ | {{https:// | ||
+ | |||
+ | |||
+ | |||
+ | {{tag> | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
home/pathogenesis/vitamind/metabolism.txt · Last modified: 09.14.2022 by 127.0.0.1
© 2015, Autoimmunity Research Foundation
All Rights Reserved. Privacy Policy